Effect of recombinant IL-33s, particularly IL-3395-270, IL-3399-270,IL-33109-270, and IL-33112-270 in HRMVECs
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE245784 | GEO | 2024/07/24
REPOSITORIES: GEO
Similar Datasets
Project description:Effect of recombinant IL-33s, particularly IL-3395-270, IL-3399-270,IL-33109-270, and IL-33112-270 in HRMVECs
| PRJNA1029963 | ENA
Project description:Intrahepatic cholestasis (IC) is a common symptom of liver diseases but with limited treatment. Huangqi decoction (HQD), a classic herbal medicine, has shown protective effects against IC. In this study, the iTRAQ-based quantitative proteomics was performed to investigate the potential mechanism of HQD on alpha-naphthylisothiocyanate (ANIT) induced IC, resulting in 2,796 quantified proteins across all the samples, including 270 differentially expressed proteins under HQD treatment. Fuzzy c-means (FCM) clustering analysis of these 270 proteins revealed that the pro-inflammatory proteins, such as LCN2, SAA1, FGG, FGA, and FGB, were assigned in the Cluster 1 (up-regulated by ANIT, and down-regulated by HQD). Following functional bioinformatics analysis and protein-protein interaction (PPI) network analysis represented that these pro-inflammatory proteins were involved in the STAT3 signaling pathway. Further real-time PCR and Western blot experiments confirmed that the expression of these proteins was consistent with the proteomic results. Moreover, HQD treatment decreased the phosphorylation of STAT3 that induced by ANIT. And Western blot experiments also revealed that HQD could decrease phosphorylation of NF-κB and down-regulate the expression inflammatory genes IL-6, and therefore inhibit IL-6/STATA3 signaling pathway. In summary, the present study suggested that HQD treatment may ameliorate intrahepatic cholestasis via inhibiting the NF-κB/IL-6/STAT3 signaling pathway.
2020-01-13 | PXD014882 | Pride
Project description:To investigate the expression prolfile of genes regulated by IL-33 in HMC3.
2024-07-24 | GSE245785 | GEO
Project description:IL-33 is a nuclear cytokine from the IL-1 family that plays important roles in health and disease.Under healthy conditions, IL-33 is constitutively expressed to high levels in the nucleus of producing cells in various human and mouse tissues. The extracellular function of IL-33 cytokine has been well documented, but it remains unclear whether intracellular nuclear IL-33 has additional functions in the nucleus. Here, we used a global proteomic approach based on quantification of 5000 individual proteins by high-resolution mass spectrometry to compare the extracellular and intracellular roles of IL-33 in primary human endothelial cells, a major source of IL-33 protein in human tissues. Large-scale analysis of protein expression was performed either after stimulation of the cells with the IL-33 mature form IL-3395-270 (during 6h or 24h) or after siRNA knockdown of intracellular IL-33 (two experiments, each with a different pool of distinct siRNAs, noted siRNA1 and siRNA2). In each case, proteins were fractionated by 1D SDS-PAGE in 12 gel bands, and label-free quantitative analysis was performed. The present dataset corresponds to the stimulation of human endothelial cells with IL-3395-270 during 6h (IL33_6) or 24h (IL33_24). Cells cultured in the absence of IL-33 were used as control (CTil33). Three independent biological replicates (noted _A, _B, _C) were prepared and analyzed for each condition, leading to 9 different samples. Each of them was fractionated into 12 gel bands analyzed by nanoLC-MS/MS, leading to 108 raw files.
2016-10-10 | PXD004117 | Pride
Project description:Background: Biological interpretation of gene expression data may differ depending on underlying assumptions and statistical tests used by the chosen bioinformatic tool. We used Gene Set Enrichment Analysis (GSEA) and Ingenuity Pathway Analysis (IPA) to analyze previously generated gene expression profiles induced in human monocytes by N. meningitidis and IL-10 (“the model system”), and by meningococcal sepsis plasma before and after immunodepletion of IL-10 (“the patient plasma system”). The objectives were to compare whether these two methods resulted in similar biological interpretation of the datasets; and identify whether GSEA provided additional insight about the human monocyte host response to meningococcal activation. Results: In both experimental models, GSEA and IPA associated genes induced in monocytes by N. meningitidis with pro-inflammatory innate immune activation, including TNF-signaling, Toll-like receptor signaling, JAK-STAT-signaling, type I and type II interferon. GSEA associated genes regulated by the presence of IL-10 with similar gene sets in both the model system and the patient plasma system. In the model system, GSEA and IPA identified 170 genes associated with oxidative phosphorylation/mitochondrial function to be down-regulated in monocytes stimulated with meningococci. In the patient plasma system, GSEA and IPA combined identified 122 genes associated with oxidative phosphorylation/mitochondrial dysfunction to be down-regulated by meningococcal sepsis plasma depleted for IL-10. Combining analyses from GSEA and IPA identified that some genes associated with oxidative phosphorylation/mitochondrial function that were inhibited by N. meningitidis were partially up-regulated by IL-10. Conclusions: Biological processes associated with the gene expression changes in the model system of meningococcal sepsis was comparable to the results found in the patient plasma system. By combining GSEA with IPA, we have discovered an inhibitory effect exerted by N. meningitidis on genes associated with oxidative phosphorylation, and that IL-10 possibly partially dampen this strong inhibitory effect, thereby identifying, to our knowledge, yet another area where IL-10 regulates the effect of LPS. We suggest that relying on a single bioinformatic tool together with arbitrarily chosen filtering criteria for data analysis may result in overlooking relevant biological processes and signaling pathways associated with genes differentially expressed between compared experimental conditions.
2016-06-08 | GSE82315 | GEO
Project description:Background: Biological interpretation of gene expression data may differ depending on underlying assumptions and statistical tests used by the chosen bioinformatic tool. We used Gene Set Enrichment Analysis (GSEA) and Ingenuity Pathway Analysis (IPA) to analyze previously generated gene expression profiles induced in human monocytes by N. meningitidis and IL-10 (“the model system”), and by meningococcal sepsis plasma before and after immunodepletion of IL-10 (“the patient plasma system”). The objectives were to compare whether these two methods resulted in similar biological interpretation of the datasets; and identify whether GSEA provided additional insight about the human monocyte host response to meningococcal activation. Results: In both experimental models, GSEA and IPA associated genes induced in monocytes by N. meningitidis with pro-inflammatory innate immune activation, including TNF-signaling, Toll-like receptor signaling, JAK-STAT-signaling, type I and type II interferon. GSEA associated genes regulated by the presence of IL-10 with similar gene sets in both the model system and the patient plasma system. In the model system, GSEA and IPA identified 170 genes associated with oxidative phosphorylation/mitochondrial function to be down-regulated in monocytes stimulated with meningococci. In the patient plasma system, GSEA and IPA combined identified 122 genes associated with oxidative phosphorylation/mitochondrial dysfunction to be down-regulated by meningococcal sepsis plasma depleted for IL-10. Combining analyses from GSEA and IPA identified that some genes associated with oxidative phosphorylation/mitochondrial function that were inhibited by N. meningitidis were partially up-regulated by IL-10. Conclusions: Biological processes associated with the gene expression changes in the model system of meningococcal sepsis was comparable to the results found in the patient plasma system. By combining GSEA with IPA, we have discovered an inhibitory effect exerted by N. meningitidis on genes associated with oxidative phosphorylation, and that IL-10 possibly partially dampen this strong inhibitory effect, thereby identifying, to our knowledge, yet another area where IL-10 regulates the effect of LPS. We suggest that relying on a single bioinformatic tool together with arbitrarily chosen filtering criteria for data analysis may result in overlooking relevant biological processes and signaling pathways associated with genes differentially expressed between compared experimental conditions.
2016-06-08 | GSE82166 | GEO
Project description:Intervention type:DRUG. Intervention1:Huaier, Dose form:GRANULES, Route of administration:ORAL, intended dose regimen:20 to 60/day by either bulk or split for 3 months to extended term if necessary. Control intervention1:None.
Primary outcome(s): For mRNA libraries, focus on mRNA studies. Data analysis includes sequencing data processing and basic sequencing data quality control, prediction of new transcripts, differential expression analysis of genes. Gene Ontology (GO) and the KEGG pathway database are used for annotation and enrichment analysis of up-regulated genes and down-regulated genes.
For small RNA libraries, data analysis includes sequencing data process and sequencing data process QC, small RNA distribution across the genome, rRNA, tRNA, alignment with snRNA and snoRNA, construction of known miRNA expression pattern, prediction New miRNA and Study of their secondary structure Based on the expression pattern of miRNA, we perform not only GO / KEGG annotation and enrichment, but also different expression analysis.. Timepoint:RNA sequencing of 240 blood samples of 80 cases and its analysis, scheduled from June 30, 2022..
| 2612481 | ecrin-mdr-crc
Project description:To investigate IL-25 in the regulation of antivral immunity, we established Il-25 stably expressing cell lines in which each target gene has been regulated by IL-25 overexpression.
2022-11-07 | GSE217085 | GEO
Project description:RNA-seq analysis of genes regulated by IL-6 in murine articular chondrocytes
| PRJEB42367 | ENA
Project description:IL-33 is a nuclear cytokine from the IL-1 family that plays important roles in health and disease. Under healthy conditions, IL-33 is constitutively expressed to high levels in the nucleus of producing cells in various human and mouse tissues. The extracellular function of IL-33 cytokine has been well documented, but it remains unclear whether intracellular nuclear IL-33 has additional functions in the nucleus. Here, we used a global proteomic approach based on quantification of 5000 individual proteins by high-resolution mass spectrometry to compare the extracellular and intracellular roles of IL-33 in primary human endothelial cells, a major source of IL-33 protein in human tissues. Large-scale analysis of protein expression was performed either after stimulation of the cells with the IL-33 mature form IL-3395-270 (during 6h or 24h) or after siRNA knockdown of intracellular IL-33 (two experiments, each with a different pool of distinct siRNAs, noted siRNA1 and siRNA2). In each case, proteins were fractionated by 1D SDS-PAGE in 12 gel bands, and label-free quantitative analysis was performed. The present dataset contains the files for the two experiments of knockdown of endogenous nuclear IL-33 expression: - RNA silencing strategy 1. Knockdown of endogenous nuclear IL-33 expression was performed with a pool of four distinct siRNAs (Dharmacon ON-TARGETplus SMARTpool IL-33 siRNAs) that have been specifically modified for efficient silencing of the target gene with reduced off-target effects. Cells transfected with these siRNA duplexes (si1) were compared with those transfected with the provided controls (CTsi1). Three independent biological replicates (noted _A, _B, _C) were prepared and analyzed for each condition, leading to 6 different samples. Each of them was fractionated into 12 gel bands analyzed by nanoLC-MS/MS, leading to 72 raw files. - RNA silencing strategy 2. The second knockdown strategy was based on the use of an independent pool of three siRNAs targeting IL-33, predesigned by another provider using new and critical siRNA design rules (Sigma MISSION Predesigned Il-33 siRNAs based on Rosetta siRNA design algorithm). Cells transfected with these siRNA duplexes (si2) were compared with those transfected with the provided controls (CTsi2). Three independent biological replicates (noted _A, _B, _C) were prepared and analyzed for each condition, leading to 6 different samples. Each of them was fractionated into 12 gel bands analyzed by nanoLC-MS/MS, leading to 72 raw files.
2016-10-12 | PXD004141 | Pride